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Ionic interactions in acetylcholine contraction of the denervated rat diaphragm
Author(s) -
FREEMAN SHIRLEY E.,
TURNER R. J.
Publication year - 1969
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1969.tb08007.x
Subject(s) - acetylcholine , contraction (grammar) , chemistry , tetrodotoxin , procaine , biophysics , muscle contraction , acetylcholine receptor , medicine , endocrinology , postsynaptic potential , stimulation , pharmacology , biochemistry , receptor , biology
1 The nature of the drug‐receptor interaction in the acetylcholine‐induced contraction of the denervated rat diaphragm was studied both by altering the external ionic environment and by determining its drug sensitivity. 2 The response to acetylcholine was insensitive to tetrodotoxin or saxitoxin, but was abolished by procaine. 3 It was unaffected by levels of MnCl 2 sufficient to block the response of the innervated diaphragm to electrical stimulation, although higher levels reduced the response. The effect of Mn ++ on the innervated diaphragm was overcome by raising the external Ca ++ level; this was ineffective in the denervated preparation. 4 In spite of its insensitivity to tetrodotoxin the acetylcholine contraction was reduced and prolonged by low external Na+ levels. This prolongation was not found when Li + substituted for Na+. 5 Increasing the external level of Ca ++ or Mg ++ 3 to 5‐fold reduced the acetylcholine contraction; high Ca ++ also prolonged it. Reduction in the divalent cation level was without effect. 6 Procaine inhibition of the acetylcholine response was largely competitive, as was inhibition due to (+)‐tubocurarine. This was shown by probit analysis and the dose‐ratio test. 7 Thiocyanate (12 m m ) augmented and prolonged the contraction; this action was modified by altering the Ca ++ or Mg ++ level of the solution. 8 The acetylcholine receptor resembles that of the innervated postsynaptic membrane.